Spigelian Hernia (SH) is an uncommon anterior abdominal wall defect, it represents 0.1%</span><span style="font-family:""> </span><span style="font-family:Verdana;">-&l...Spigelian Hernia (SH) is an uncommon anterior abdominal wall defect, it represents 0.1%</span><span style="font-family:""> </span><span style="font-family:Verdana;">-</span><span style="font-family:""> </span><span style="font-family:Verdana;">2% of all abdominal wall hernias. SHs have been traditionally repaired by open technique, but laparoscopic approaches are becoming more common and widely described in the literature. Here we present a case report of a 69-year-old woman who presented with abdominal pain, nausea, abdominal distention and absence of bowel movements for 2 days. A computed tomography performed in an external facility revealed a right-sided and incarcerated SH containing bowel and mesentery. The patient was treated surgically and the abdominal wall defect was repaired by a laparoscopic transabdominal preperitoneal (TAPP) approach. The patient was discharged 24 hours after surgery in excellent conditions. We hold that the TAPP approach is anatomically the soundest repair, with all the added benefits of minimally invasive surgery.展开更多
Deficiencies in DNA repair due to inherited germ-line mutations in DNA repair genes cause increased risk of gastrointestinal(GI) cancer. In sporadic GI cancers, mutations in DNA repair genes are relatively rare. Howev...Deficiencies in DNA repair due to inherited germ-line mutations in DNA repair genes cause increased risk of gastrointestinal(GI) cancer. In sporadic GI cancers, mutations in DNA repair genes are relatively rare. However, epigenetic alterations that reduce expression of DNA repair genes are frequent in sporadic GI cancers. These epigenetic reductions are also found in field defects that give rise to cancers. Reduced DNA repair likely allows excessive DNA damages to accumulate in somatic cells. Then either inaccurate translesion synthesis past the un-repaired DNA damages or error-prone DNA repair can cause mutations. Erroneous DNA repair can also cause epigenetic alterations(i.e., epimutations, transmitted through multiple replication cycles). Some of these mutations and epimutations may cause progression to cancer. Thus, deficient or absent DNA repair is likely an important underlying cause of cancer. Whole genome sequencing of GI cancers show that between thousands to hundreds of thousands of mutations occur in these cancers. Epimutations that reduce DNA repair gene expression and occur early in progression to GI cancers are a likely source of this high genomic instability. Cancer cells deficient in DNA repair are more vulnerable than normal cells to inactivation by DNA damaging agents. Thus, some of the most clinically effective chemotherapeutic agents in cancer treatment are DNA damaging agents, and their effectiveness often depends on deficient DNA repair in cancer cells. Recently, at least 18 DNA repair proteins, each active in one of six DNA repair pathways, were found to be subject to epigenetic reduction of expression in GI cancers. Different DNA repair pathways repair different types of DNA damage. Evaluation of which DNA repair pathway(s) are deficient in particular types of GI cancer and/or particular patients may prove useful in guiding choice of therapeutic agents in cancer therapy.展开更多
目的分析耳内镜下内衬法鼓膜修补与耳内镜下蝶形软骨膜嵌入法鼓膜修补的应用差异性。方法选取2021年12月至2023年12月我院收治的50例慢性化脓性中耳炎鼓膜穿孔者为研究对象,采用随机对照表法分为观察组和对照组各25例。观察组采取耳内...目的分析耳内镜下内衬法鼓膜修补与耳内镜下蝶形软骨膜嵌入法鼓膜修补的应用差异性。方法选取2021年12月至2023年12月我院收治的50例慢性化脓性中耳炎鼓膜穿孔者为研究对象,采用随机对照表法分为观察组和对照组各25例。观察组采取耳内镜下内衬法鼓膜修补,对照组采取耳内镜下蝶形软骨膜嵌入法鼓膜修补术,比较两组患者治疗后鼓膜愈合率、术中出血量及手术时间、手术并发症(移植物感染、鼓膜内陷、鼓膜炎),分析两组术前、术后2个月平均气导听阈(PTA)、气骨导差(ABG)评分、术后24 h VAS评分。结果治疗后,观察组鼓膜愈合率、术中出血量与对照组比较,差异无统计学意义(P>0.05);观察组手术时间显著短于对照组,差异有统计学意义(P<0.05);治疗前,两组PTA、ABG比较,无明显差异(P>0.05);治疗后,观察组优于对照组,差异有统计学意义(P<0.05);治疗前两组VAS评分比较,无明显差异(P>0.05),治疗后,观察组优于对照组,差异有统计学意义(P<0.05);观察组并发症发生情况低于对照组,差异有统计学意义(P<0.05)。结论在耳内镜下内衬法鼓膜修补术较蝶形软骨膜嵌入法鼓膜修补治疗优势更明显,可改善听力,减轻疼痛程度,且手术时间较短,有利于减少术中出血,提高鼓膜愈合率,还可降低术后并发症发生率,效果明显。展开更多
文摘Spigelian Hernia (SH) is an uncommon anterior abdominal wall defect, it represents 0.1%</span><span style="font-family:""> </span><span style="font-family:Verdana;">-</span><span style="font-family:""> </span><span style="font-family:Verdana;">2% of all abdominal wall hernias. SHs have been traditionally repaired by open technique, but laparoscopic approaches are becoming more common and widely described in the literature. Here we present a case report of a 69-year-old woman who presented with abdominal pain, nausea, abdominal distention and absence of bowel movements for 2 days. A computed tomography performed in an external facility revealed a right-sided and incarcerated SH containing bowel and mesentery. The patient was treated surgically and the abdominal wall defect was repaired by a laparoscopic transabdominal preperitoneal (TAPP) approach. The patient was discharged 24 hours after surgery in excellent conditions. We hold that the TAPP approach is anatomically the soundest repair, with all the added benefits of minimally invasive surgery.
文摘Deficiencies in DNA repair due to inherited germ-line mutations in DNA repair genes cause increased risk of gastrointestinal(GI) cancer. In sporadic GI cancers, mutations in DNA repair genes are relatively rare. However, epigenetic alterations that reduce expression of DNA repair genes are frequent in sporadic GI cancers. These epigenetic reductions are also found in field defects that give rise to cancers. Reduced DNA repair likely allows excessive DNA damages to accumulate in somatic cells. Then either inaccurate translesion synthesis past the un-repaired DNA damages or error-prone DNA repair can cause mutations. Erroneous DNA repair can also cause epigenetic alterations(i.e., epimutations, transmitted through multiple replication cycles). Some of these mutations and epimutations may cause progression to cancer. Thus, deficient or absent DNA repair is likely an important underlying cause of cancer. Whole genome sequencing of GI cancers show that between thousands to hundreds of thousands of mutations occur in these cancers. Epimutations that reduce DNA repair gene expression and occur early in progression to GI cancers are a likely source of this high genomic instability. Cancer cells deficient in DNA repair are more vulnerable than normal cells to inactivation by DNA damaging agents. Thus, some of the most clinically effective chemotherapeutic agents in cancer treatment are DNA damaging agents, and their effectiveness often depends on deficient DNA repair in cancer cells. Recently, at least 18 DNA repair proteins, each active in one of six DNA repair pathways, were found to be subject to epigenetic reduction of expression in GI cancers. Different DNA repair pathways repair different types of DNA damage. Evaluation of which DNA repair pathway(s) are deficient in particular types of GI cancer and/or particular patients may prove useful in guiding choice of therapeutic agents in cancer therapy.
文摘目的分析耳内镜下内衬法鼓膜修补与耳内镜下蝶形软骨膜嵌入法鼓膜修补的应用差异性。方法选取2021年12月至2023年12月我院收治的50例慢性化脓性中耳炎鼓膜穿孔者为研究对象,采用随机对照表法分为观察组和对照组各25例。观察组采取耳内镜下内衬法鼓膜修补,对照组采取耳内镜下蝶形软骨膜嵌入法鼓膜修补术,比较两组患者治疗后鼓膜愈合率、术中出血量及手术时间、手术并发症(移植物感染、鼓膜内陷、鼓膜炎),分析两组术前、术后2个月平均气导听阈(PTA)、气骨导差(ABG)评分、术后24 h VAS评分。结果治疗后,观察组鼓膜愈合率、术中出血量与对照组比较,差异无统计学意义(P>0.05);观察组手术时间显著短于对照组,差异有统计学意义(P<0.05);治疗前,两组PTA、ABG比较,无明显差异(P>0.05);治疗后,观察组优于对照组,差异有统计学意义(P<0.05);治疗前两组VAS评分比较,无明显差异(P>0.05),治疗后,观察组优于对照组,差异有统计学意义(P<0.05);观察组并发症发生情况低于对照组,差异有统计学意义(P<0.05)。结论在耳内镜下内衬法鼓膜修补术较蝶形软骨膜嵌入法鼓膜修补治疗优势更明显,可改善听力,减轻疼痛程度,且手术时间较短,有利于减少术中出血,提高鼓膜愈合率,还可降低术后并发症发生率,效果明显。
